Journal of Microbiology

Il-Sup Kim

3 Articles

Ectopic Expression of Sweet Potato MuS1 Increases Acquired Stress Tolerance and Fermentation Yield in Saccharomyces cerevisiae: Il-Sup Kim , Sun-Young Shin , Sun-Hyung Kim , Ho-Sung Yoon; J. Microbiol. 2012;50(3):544-546. Published online June 30, 2012; DOI: https://doi.org/10.1007/s12275-012-2043-3

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The MuS1 gene is highly homologous to many stress-related proteins in plants. Here, we characterized whether a new candidate gene, MuS1, is related to multiple stress tolerance in yeast as it is in plants. Transgenic yeast strain expressing MuS1 were more resistant to hydrogen peroxide, menadione, high salinity, metals (i.e., cadmium, copper, iron, and zinc), ethanol, and lactic acid than wild-type strain transformed with a vector alone. In addition, the alcohol yield of the transgenic yeast strain was higher than that of the wild-type strain during the batch fermentation process. These results show that MuS1-expressing transgenic yeast strain exhibits enhanced alcohol yield as well as tolerance to abiotic stresses, especially metal stress.

Citations

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The unique importance of sweetpotato: Insights focusing on genetic improvements of salt and drought tolerance
Mingku Zhu
Scientia Horticulturae.2025; 339: 113848. CrossRef
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Frontiers in Plant Science.2024;[Epub] CrossRef

Adaptive Stress Response to Menadione-Induced Oxidative Stress in Saccharomyces cerevisiae KNU5377: Il-Sup Kim , Ho-Yong Sohn , Ingnyol Jin; J. Microbiol. 2011;49(5):816-823. Published online November 9, 2011; DOI: https://doi.org/10.1007/s12275-011-1154-6

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Abstract PDF

The molecular mechanisms involved in the ability of yeast cells to adapt and respond to oxidative stress are of great interest to the pharmaceutical, medical, food, and fermentation industries. In this study, we investigated the time-dependent, cellular redox homeostasis ability to adapt to menadione-induced oxidative stress, using biochemical and proteomic approaches in Saccharomyces cerevisiae KNU5377. Time-dependent cell viability was inversely proportional to endogenous amounts of ROS measured by a fluorescence assay with 2′,7′-dichlorofluorescin diacetate (DCFHDA), and was hypersensitive when cells were exposed to the compound for 60 min. Morphological changes, protein oxidation and lipid peroxidation were also observed. To overcome the unfavorable conditions due to the presence of menadione, yeast cells activated a variety of cell rescue proteins including antioxidant enzymes, molecular chaperones, energy-generating metabolic enzymes, and antioxidant molecules such as trehalose. Thus, these results show that menadione causes ROS generation and high accumulation of cellular ROS levels, which affects cell viability and cell morphology and there is a correlation between resistance to menadione and the high induction of cell rescue proteins after cells enter into this physiological state, which provides a clue about the complex and dynamic stress response in yeast cells.

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Heat Shock Causes Oxidative Stress and Induces a Variety of Cell Rescue Proteins in Saccharomyces cerevisiae KNU5377: Il-Sup Kim , Hye-Youn Moon , Hae-Sun Yun , Ingnyol Jin; J. Microbiol. 2006;44(5):492-501.; DOI: https://doi.org/2449 [pii]

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Abstract PDF: In this study, we attempted to characterize the physiological response to oxidative stress by heat shock in Saccharomyces cerevisiae KNU5377 (KNU5377) that ferments at a temperature of 40°C. The KNU5377 strain evidenced a very similar growth rate at 40°C as was recorded under normal conditions. Unlike the laboratory strains of S. cerevisiae, the cell viability of KNU5377 was affected slightly under 2 hours of heat stress conditions at 43°C. KNU5377 evidenced a time-dependent increase in hydroperoxide levels, carbonyl contents, and malondialdehyde (MDA), which increased in the expression of a variety of cell rescue proteins containing Hsp104p, Ssap, Hsp30p, Sod1p, catalase, glutathione reductase, G6PDH, thioredoxin, thioredoxin peroxidase (Tsa1p), Adhp, Aldp, trehalose and glycogen at high temperature. Pma1/2p, Hsp90p and H+-ATPase expression levels were reduced as the result of exposure to heat shock. With regard to cellular fatty acid composition, levels of unsaturated fatty acids (USFAs) were increased significantly at high temperatures (43°C), and this was particularly true of oleic acid (C18:1). The results of this study indicated that oxidative stress as the result of heat shock may induce a more profound stimulation of trehalose, antioxidant enzymes, and heat shock proteins, as well as an increase in the USFAs ratios. This might contribute to cellular protective functions for the maintenance of cellular homeostasis, and may also contribute to membrane fluidity.

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